Signal transduction within the nucleus: Revisiting phosphoinositide inositide-specific phospholipase Cbeta(1).

The existence of both polyphosphoinositides and the enzymes responsible for their metabolism inside the nucleus is well established and clearly indicates that they constitute an autonomous lipid-dependent signaling system, independently regulated from its plasma membrane counterpart and modulated during both cell cycle progression and differentiation. PI–PLCb1 is a key player in the regulation of nuclear inositol lipid signaling and, given that PI–PLC catalyzes PtdIns(4,5)P2 hydrolysis, its enzymatic function could be involved also in chromatin remodeling, that is somehow PtdIns(4,5)P2-dependent. Indeed we have focused our attention on the most recent findings hinting at an involvement of PtdIns(4,5)P2 in nuclear structure, i.e. chromatin organization, as well as on emerging data dealing with specific targets of PI–PLCb1. Moreover, we have addressed the issue of PI–PLCb1 and neoplastic cell growth and namely the evidence which links the monoallelic deletion of PI–PLCb1 to the evolution of MDS in acute myeloid leukemia AML